Central sleep apnea (CSA) is a condition characterized by periodic temporary cessation of normal respiration. Central sleep apnea is differentiated from other categories of apneas, such as obstructive sleep apnea, by having a neurological rather than a structural origin. In episodes of CSA, nerve stimulation to the diaphragm temporarily decreases to the point that the afflicted person's diaphragm fails to properly contract thus failing to inspire. As the person's metabolism proceeds leading to an increasing metabolic need for respiration, the person becomes partially aroused interrupting the apneic episode with respiration. The respiration immediately following an apneic episode frequently is of hyperventilatory nature and recurrent episodes of CSA and hyperventilation disrupts the person's restful sleep. Alternating episodes of CSA and hyperventilation and consequent swings in sympathetic drive are also found in patients experiencing some degree of heart failure (HF) and these episodes of CSA, in addition to being disruptive of the patient's sleep, also tend to worsen the persons HF. Thus, it will be appreciated that there is a need for detection and therapeutic treatment for patients suffering from CSA.
As CSA involves a temporary cessation of normal respiration, one method of detecting CSA is to observe the patient's respiration and detect an occurrence of an excessive delay of the initiation of an inspiration cycle. For example, an impedance sensor arranged to measure the patient's transthoracic impedance can measure the cyclic variations in the transthoracic impedance as the lungs are filled and emptied through the breathing cycle. Sensors can also be arranged about the patient's thorax to detect the expansion and contraction of the chest cavity throughout the respiration cycle. However, these methods actually measure the patient's respiratory response rather than the driving neurological demand and are somewhat susceptible to erroneous measurements, for example due to patient movement during sleep. The phrenic nerves conduct respiratory demand signals from the brain to the left and right sides of the diaphragm and sensing activity on the phrenic nerves could provide the ability to directly sense the patient's respiratory demand rather than inferring this demand based on measurements of the respiratory response.
Sensing phrenic nerve signals are known in some implantable medical device applications. For example, U.S. Pat. No. 5,483,969 to Testerman et al. discloses a system for measuring phrenic nerve activity in order to apply appropriate sleep apnea therapy. However, the manner in which known implantable medical devices monitor nerve activity, such as phrenic nerve activity, is generally not conducive for use in many implantable medical device applications, particularly those intended for long-term implantation. In particular, in order to accurately assess nerve signals, band pass filtering and relatively high-rate sampling, such as on the order of 30 kHz, must typically be performed to accurately sense the signals. However, when the implantable medical device relies upon battery power, the use of such high-rate sampling may excessively draw on the battery and have the effect of significantly limiting the useful life of the implantable medical device before battery replacement is indicated.
Hence, there is a need for an implantable medical device that is capable of monitoring nerve activity so that the implantable medical device is better able to assess neurologically determined parameters affecting treatment afforded to patients. To this end, there is a need for a system and method that is able to accurately sense signals in a patient's nervous system in a manner that consumes less battery power.